Postjunctional alpha 2-adrenoceptors are not present in proximal arterioles of rat intestine.
The purpose of this study was to evaluate two potential stimuli for nitric oxide (NO) release in rat intestinal arterioles during sympathetic nerve activation. To determine whether these vessels contain endothelial alpha 2-adrenoceptors linked to the L-arginine-NO pathway, intravital microscopy was used to study the response of first-order arterioles (1As, 20-40 microns ID) to direct application of 1) the selective alpha 2-agonist BHT-933 and 2) norepinephrine (NE) or sympathetic nerve stimulation before and after alpha 1- or alpha 2-receptor blockade. The effect of sympathetic nerve stimulation on 1A wall shear rate (WSR) was also determined to evaluate the possibility of hemodynamic shear stress as a stimulus for NO release. BHT-933 had no effect on 1A diameter, whereas NE produced dose-dependent constrictions of 5 +/- 3 to 15 +/- 3 microns, which were usually abolished by the alpha 1-antagonist prazosin but unaffected by the alpha 2-antagonist idazoxan. Sympathetic nerve stimulation at 3, 8, and 16 Hz induced constrictions of 4 +/- 1, 8 +/- 2, and 17 +/- 4 microns, respectively, and these constrictions were also usually abolished by prazosin but unaffected by idazoxan. Resting WSR averaged 1,997 +/- 163 s-1 and decreased to 1,587 +/- 209, 1,087 +/- 195, and 537 +/- 99 s-1 during 3-, 8-, and 16-Hz nerve stimulation. These results suggest that alpha 2-adrenoceptor-dependent pathways do not influence either resting tone or sympathetic constriction of proximal arterioles in the intestinal submucosa and that luminal shear stress in these vessels significantly decreases with sympathetic constriction. It therefore appears unlikely that either alpha 2-receptor activation or changes in hemodynamic shear serve as stimuli for arteriolar NO release during periods of increased sympathetic nerve activity.
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Department of Physiology, West Virginia University School of Medicine, Morgantown 26506-9229, USA.
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D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D001381:Azepines / Q000494:pharmacology*; D001783:Blood Flow Velocity / Q000187:drug effects; D004558:Electric Stimulation; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D004912:Erythrocytes / Q000502:physiology; D007421:Intestine, Small / Q000098:blood supply* / Q000294:innervation; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects
D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D001381:Azepines; D018341:Receptors, Adrenergic, alpha-2; D009569:Nitric Oxide; C015603:azepexole; D019001:Nitric Oxide Synthase; D009638:Norepinephrine